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11 results on '"Arreto, C.-D."'

9. Thromboxane A2 accounts for bronchoconstriction but not for platelet sequestration and microvascular albumin exchanges induced by fMLP in the guinea pig lung.

Author

Bureau, M F, De Clerck, F, Lefort, J, Arreto, C D, and Vargaftig, B B

Abstract

When injected i.v. to guinea pigs, the granulocyte secretagog N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) induces bronchoconstriction (BC), lung platelet sequestration and increased transendothelial albumin exchanges in lungs. We evaluated BC and the variations of the lung contents in radiolabeled platelets, erythrocytes and extravascular albumin, as measurements of platelet lung entrapment, reduction of lung blood volume and increase of transendothelial albumin exchanges, respectively. Trimetoquinol, a thromboxane A2 (TXA2)-endoperoxide receptor antagonist, inhibited BC and platelet entrapment by lungs induced by fMLP, but protection was nonspecific because it also suppressed BC by histamine. The specific TXA2 synthetase inhibitor/endoperoxide receptor antagonist ridogrel suppressed BC and reduced lung platelet entrapment, but failed to prevent the increase of extravascular albumin and the decrease of erythrocyte lung contents due to fMLP. Consequently, the fMLP-induced increase of vascular albumin exchanges and reduction of lung blood volume are TXA2-independent. Aspirin prevented BC, but failed to suppress lung platelet entrapment by fMLP, indicating that in vivo platelet activation is not TXA2-dependent, even though the levels of circulating TXB2, the stable metabolite of TXA2, were increased after fMLP concomitantly with that of 6-keto-prostaglandin (PG)F1 alpha, the stable metabolite of PGI2. The ridogrel-treated animals showed reduced blood level of TXB2 and increased levels of 6-keto-PGF1 alpha after fMLP challenge. Blocking the cyclooxygenase pathway with aspirin prevented ridogrel-induced protection against lung platelet sequestration after fMLP, supporting the concept that rechanneling of arachidonate metabolism toward protective prostaglandins accounts for protection by ridogrel.

Published
1992

10. Pharmacological differentiation by pertussis toxin of the in vivo acute responses to fMLP and PAF in guinea-pig lungs.

Author

Arreto CD, Bureau MF, Imaizumi A, and Vargaftig BB

Subjects
Acetylcholine pharmacology, Animals, Blood Platelets drug effects, Blood Volume drug effects, Capillary Permeability drug effects, Female, Guinea Pigs, Leukocytes drug effects, Leukopenia drug therapy, Male, Thrombocytopenia chemically induced, Bronchoconstriction drug effects, Lung drug effects, N-Formylmethionine Leucyl-Phenylalanine antagonists & inhibitors, Pertussis Toxin, Platelet Activating Factor pharmacology, Virulence Factors, Bordetella pharmacology
Abstract

1. The effects of pertussis toxin on the N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) and platelet-activating factor (PAF)-induced variations in pulmonary capillary albumin exchanges, blood volume, leucocyte or platelet sequestration were studied in the guinea-pig, by use of radioactive tracers. The effects of pertussis toxin on pulmonary insufflation pressure were studied in parallel. 2. The i.v. administration of fMLP and PAF to the guinea-pig was followed by bronchoconstriction, increased lung capillary albumin exchanges (vasopermeability) sequestration of leucocytes, leucopenia and reduction of blood volume (vasoconstriction). PAF also induced platelet sequestration in lungs and thrombocytopenia. 3. Pertussis toxin (10 micrograms kg-1, i.v., 72 h before the experiment) prevented all the studied fMLP-induced effects, but failed to modify PAF-induced bronchoconstriction, lung vasoconstriction, platelet sequestration, thrombocytopenia and the increased capillary vasopermeability. In the same conditions the lung leucocyte sequestration was not significantly affected when leucopenia was partially reduced. 4. It is suggested that the effects of fMLP, but not those of PAF, involve a Gi-like protein.

Published
1993
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11. [Effect of chlorhexidine on bacterial fibrinolytic and collagenolytic activity].

Author

Pellat B, Arreto CD, and Vandermander J

Subjects
Bacteroides enzymology, Collagen metabolism, Dental Plaque microbiology, Fibronectins metabolism, Humans, Periodontal Diseases microbiology, Chlorhexidine therapeutic use, Dental Plaque enzymology, Periodontal Diseases enzymology, Protease Inhibitors therapeutic use
Abstract

Destructive periodontal diseases are characterized by tissue breakdown partly mediated by various enzymes originating from bacteria and/or tissue. Collagen and fibronectin are two of the main substrates available for enzyme activity. Since chlorhexidine is largely used during and after periodontal therapy, we have investigated the effects of chlorhexidine upon some bacterial proteases. Our data indicate that chlorhexidine inhibits, on a dose-dependent manner, both fibronectin and collagen hydrolysis mediated by either bacteroides (porphyromonas) gingivalis or bacteroides intermedius. Thus, it might be hypothesized that a side from its bactericidal activity, chlorhexidine helps to prevent periodontal tissue destruction directly by enzyme inhibition.

Published
1991

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